ArticleProtein & cell2016
Loss of IκB kinase β promotes myofibroblast transformation and senescence through activation of the ROS-TGFβ autocrine loop.
Article in Protein & cell, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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Who cites it
9 citing papers in PubMed, 11 citations in OpenAlex.
- CT-sensitized nanoprobe for effective early diagnosis and treatment of pulmonary fibrosis.Journal of nanobiotechnology · 2025Article
- The TGFβ2-Snail1-miRNAClinical and translational medicine · 2024Article
- Reactive oxygen species (ROS) scavenging biomaterials for anti-inflammatory diseases: from mechanism to therapy.Journal of hematology & oncology · 2023Review
- TGF-β as A Master Regulator of Aging-Associated Tissue Fibrosis.Aging and disease · 2023Review
- Fibroblast-specific IKK-β deficiency ameliorates angiotensin II-induced adverse cardiac remodeling in mice.JCI insight · 2021Article
- Sirtuin 3 is essential for hypertension-induced cardiac fibrosis via mediating pericyte transition.Journal of cellular and molecular medicine · 2020Article
- LATS1/2 suppress NFκB and aberrant EMT initiation to permit pancreatic progenitor differentiation.PLoS biology · 2019Article
- Vascular progenitor cell senescence in patients with Marfan syndrome.Journal of cellular and molecular medicine · 2019Article
- Characterizing the "POAGome": A bioinformatics-driven approach to primary open-angle glaucoma.Progress in retinal and eye research · 2017Review
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
Abstract
Using forward and reverse genetics and global gene expression analyses, we explored the crosstalk between the IκB kinase β (IKKβ) and the transforming growth factor β (TGFβ) signaling pathways. We show that in vitro ablation of Ikkβ in fibroblasts led to progressive ROS accumulation and TGFβ activation, and ultimately accelerated cell migration, fibroblast-myofibroblast transformation and senescence. Mechanistically, the basal IKKβ activity was required for anti-oxidant gene expression and redox homeostasis. Lacking this activity, IKKβ-null cells showed ROS accumulation and activation of stress-sensitive transcription factor AP-1/c-Jun. AP-1/c-Jun activation led to up-regulation of the Tgfβ2 promoter, which in turn further potentiated intracellular ROS through the induction of NADPH oxidase (NOX). These data suggest that by blocking the autocrine amplification of a ROS-TGFβ loop IKKβ plays a crucial role in the prevention of fibroblast-myofibroblast transformation and senescence.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.